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      Nitric-Oxide-Related and Non-Related Mechanisms in the Acetylcholine-Evoked Relaxations in Cat Femoral Arteries


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          The possible contribution of nitric oxide (NO) and other endothelial factors to the vasodilatation induced by acetylcholine (ACh) was analyzed in cat femoral arteries. For this purpose, the modifications by different treatments of ACh-induced relaxations were compared with those of exogenous NO-induced relaxations. Although the ACh-induced endothelium-dependent relaxation was not affected by the cyclooxygenase inhibitor indomethacin, it was partially inhibited by the lipoxygenase blocker 5,8,11,14-eicosatetraenoic acid, and by the NO inactivators phenidone, hydroquinone and oxyhemoglobin (OxHb). Additionally, this type of relaxation was reduced by the NO-synthase inhibitor N<sup>G</sup>-monomethyl- L-arginine (L·NMMA) and abolished by N<sup>G</sup>-nitro- L-arginine methyl ester; these later effects were selectively antagonized by L-arginine. Exogenous NO-induced vasodilatations were abolished by OxHb and unmodified by L-NMMA. Blocking sodium pump activity decreased vasodilatations to ACh, NO, sodium nitroprusside and 8-bromoguanosine 3’,5’-cyclic monophosphate. 4-Aminopyridine, a K<sup>+</sup> channel antagonist, reduced the relaxation induced by ACh but not that induced by exogenous NO. These results suggest: (1) ACh-induced relaxation in these vessels is mainly due to endothelial cell NO release; (2) NO does not act on 4-AP-sensitive K<sup>+</sup> channels, although these channels may be involved in NO release from the endothelium, and (3) one of the relaxant mechanisms of NO could be the activation of the vascular sodium pump.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 30
          : 6
          : 339-347
          Departamento de Farmacología y Terapéutica, Facultad de Medicina de la Universidad Autónoma, Madrid, España
          159016 J Vasc Res 1993;30:339–347
          © 1993 S. Karger AG, Basel

          Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

          : 26 November 1992
          : 08 June 1993
          Page count
          Pages: 9
          Research Paper

          General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
          Acetylcholine,Cat femoral arteries,Nitric oxide,Endothelium,Relaxation


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